NURS 165 Study Guide - Final Guide: Diastole, Combined Oral Contraceptive Pill, Coronary Occlusion
Thromboembolism and ACS – Pathophysiology
• Hemostasis – arrest of bleeding, explosive positive-feedback of platelets,
clotting factors, and endothelial cells
o Under normal circumstances, clotting only occurs when and where it
is needed to stop bleeding/hemorrhage
o Normal Hemostasis:
▪ Vascular injury → local neurohumoral factors cause
vasoconstriction → platelets bind via glycoprotein 1b to von
Willebrand factor → released ADP and thromboxane A
promote platelet aggregation via glycoprotein 2b to fibrinogen
→ forms primary hemostatic plug → cascade solidifies plug &
becomes secondary hemostatic plug → Counterregulatory
mechanisms link to injury
o Platelets have short lifespan (5-10 days)
▪ Normal count is 150-400 thousand per microliter
▪ Exposure to collagen via von Willebrand factor is activation
• Collagen = something’s exposed, meaning injury
• Key players in hemostasis
o vWF: links platelet to subendothelial collagen exposed on damaged
endothelium
o Gp1b: platelet surface; acts as receptor for vWF
o Fibrinogen: permits adjoining platelets; aggregation
o Gp2b: receptor for fibrinogen; aggregation
o Thromboxane and ADP: promote aggregation
o Function of clotting factors
▪ Intrinsic pathway – Hageman factor contacts subendothelium
▪ Extrinsic – tissue factor released by damaged cells
• Expressed by cells not normally exposed to flowing
blood, like subendothelium. Damage to blood vessel
can expose TF.
• The Clotting Cascade Proteins:
o Proteases:
▪ 7, 9, 11 – extrinsic
▪ 10 – common pathway, activates thrombin
o Cofactors:
▪ 5 and 8
▪ Help protease enzyme activity do their job
o Regulatory Proteins
▪ C and S
o Clot is made from FIBRIN
▪ Thrombin plays a really key role though! It cleaves peptides off
fibrinogen, converting it to fibrin.
▪ Fibrin is insoluble → fibrin molecules adhere to one another →
spongy mass → hardens to form blood clot
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• Antithrombin blocks thrombin, and heparin increases
antithrombin
▪ Plasmin system breaks down clots when no longer needed
o Lab counts
▪ Platelet count
▪ Prothrombin time (PT)
• Also internationalized normal ratio (INR)
▪ D-dimer – fibrin degrade product
• Principles of Bleeding & Clotting disorders
o Hemostasis – balance of pro & anti clotting forces
▪ Pro: expsed collagen, vWF, platelets
▪ Anti: intact endothelium NO, protein C to inactivate factor V
o Clotting should be
▪ Localized!
▪ Freely available always!
• You know in case trauma happens
▪ Stopped when not needed!
o Pathophysiology
▪ Excessive bleeding – hypocoaguable
▪ Excessive clotting – hypercoaguable
o Hypocoaguable states
▪ Bleeding disorders
▪ Platelet deficiencies – inc. bleeding
▪ Examples
• Von Willebrand disease – abnormal platelet adhesion
• Hemophilia – decreased factor 7 or 9
• Heparin-induced thrombocytopenia
o Too few platelets
o Hypercoagulable states
▪ Deficient/abnormal clotting factors
▪ Excessive clotting factors
▪ Examples
• Factor V Leiden – protein C resistance
find more resources at oneclass.com
find more resources at oneclass.com
